Esnault V, Delcroix C, Dubigeon P, Guenel J
Service de Médecine IV-Néphrologie, C.H.U., Nantes.
Nephrologie. 1988;9(6):277-80.
Intratubular deposits of calcium oxalate crystals can be responsible for acute renal failure. The present report concerns two cases for which none of the known causes of oxalate nephropathy were found. Both patients had common features: chronic alcoholism and denutrition. Except for early lumbar and abdominal pain, the renal failure picture was without any peculiarity. Renal biopsy showed tubular epithelium alterations with marked luminal deposition of birefringent crystals consistent with calcium oxalate. In one patient serum oxalate level was high, and in the other urinary oxalate excretion rose above normal when diuresis resumed. Renal function recovered spontaneously (follow-up of four years for one patient). Neither intoxication nor intestinal disease could be detected. Given the key role of pyridoxine in oxalate metabolism, we suggest that vitamin B6 deficiency secondary to alcoholism and denutrition could cause a rise in oxalemia leading to oxalate nephropathy. Experiments in animals support this hypothesis.
草酸钙晶体的肾小管内沉积可导致急性肾衰竭。本报告涉及两例未发现已知草酸肾病病因的病例。两名患者有共同特征：慢性酒精中毒和营养不良。除了早期的腰腹痛外，肾衰竭表现并无任何特殊之处。肾活检显示肾小管上皮细胞改变，管腔内有大量双折射晶体沉积，符合草酸钙特征。一名患者血清草酸水平升高，另一名患者在利尿恢复时尿草酸排泄量高于正常水平。肾功能自发恢复（一名患者随访四年）。未检测到中毒或肠道疾病。鉴于吡哆醇在草酸代谢中的关键作用，我们认为酒精中毒和营养不良继发的维生素B6缺乏可能导致草酸血症升高，进而引发草酸肾病。动物实验支持这一假说。
